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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The objectives of the present study were to determine whether an intracisternal injection of fibrinogen-sodium citrate, a model of neurogenic pulmonary edema (NPE), produces protein-rich or protein-poor pulmonary edema, and to determine whether the edema is associated with pulmonary vascular hypertension and pulmonary congestion. Fibrinogen (6-10 mg/ml) dissolved in 0.055 M sodium citrate was injected into the cisterna magna of six New Zealand White rabbits. Six additional rabbits were injected with saline to control for the effects of intracranial hypertension and pulmonary vascular hypertension. The fibrinogen-sodium citrate solution or sodium citrate alone, as opposed to saline, produced systemic and pulmonary vascular hypertension, pulmonary edema, hypoxemia, hypercapnia, and acidosis. The lungs from fibrinogen-injected rabbits were edematous, congested, and liverlike in appearance. Tracheal froth that was blood tinged and protein rich was present in five of the six rabbits. Microscopic examination of lung biopsies revealed erythrocytes and plasma in the alveoli and focal injury to the pulmonary microvascular endothelium. Fibrinogen-sodium citrate increased (P less than 0.05) the extravascular lung water (EVLW) (10.3 +/- 2.0 vs. 5.5 +/- 0.6 g, means +/- SE), lung blood weight (9.7 +/- 1.3 vs. 3.8 +/- 0.6 g), total dry lung weight (3.2 +/- 0.4 vs. 2.0 +/- 0.1 g), and the EVLW-to-blood-free dry lung weight ratio (7.0 +/- 0.8 vs. 4.0 +/- 0.3 g) from saline-control values. There was no difference in the blood-fre dry lung weight (1.4 +/- 0.1 vs. 1.3 +/- 0.1 g) between the two groups. These findings demonstrate that pulmonary congestion, pulmonary vascular hypertension, and focal endothelial injury contribute to the development of NPE.
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PMID:Endothelial injury and pulmonary congestion characterize neurogenic pulmonary edema in rabbits. 311 22

Acetazolamide (Diamox) induced carbonic anhydrase inhibition is an efficient means of eliminating surplus water and bicarbonate in the overhydrated and alkalotic patient. Previous studies have demonstrated an unexpected and unexplained increase in arterial and venous oxygenation during acute carbonic anhydrase inhibition. In the present investigation we assessed the effect of acetazolamide 15 mg kg-1 on pulmonary gas exchange in 10 critically ill, mechanically ventilated patients. Median arterial oxygen tension increased by 0.9 kPa and central venous oxygen tension and content by 16-18% and 6-8% respectively. The improved oxygenation could, however, not be attributed to an improved pulmonary oxygen exchange as both pulmonary venous admixture (Qs Qt-1) and physiological dead space ventilation (VD VT-1) increased. The increase in arterial oxygen tension can be explained by a rightward shift of the oxyhemoglobin dissociation curve due to the increased acidity of the blood during carbonic anhydrase inhibition (Bohr effect). Acetazolamide does not depress oxygen consumption, so the increase in central venous oxygen content probably reflects an improved cardiac performance. This could conceivably be mediated via sympathetic activation in response to acetazolamide induced carbon dioxide retention.
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PMID:Respiratory function and carbonic anhydrase inhibition. 311 60

Specimens of Bufo marinus were exposed to aerial and aquatic hypercapnia (5% CO2) in a closed, water recirculation system to evaluate mechanisms involved in the compensation of a respiratory acidosis in these animals. Arterial PCO2 was elevated from about 9 mmHg (1 mmHg = 133.3 Pa) to 35 (1 h) and 37 mmHg (2 h), and gradually approached about 40 mmHg (24 h of hypercapnia). The typical hypercapnia-induced reduction in plasma pH from about 7.9 to below 7.4 was partially offset, at least during the first hours of hypercapnia, by a reduction in the inspired/arterial PCO2 difference, presumably brought about by pulmonary hyperventilation. The predominant contributor to extracellular pH compensation, however, was a net gain of bicarbonate from the environment, mainly facilitated by ammonia excretion. Bicarbonate originating from the environment was accumulated in the body fluids, increasing the plasma concentration from the control of about 9 to 36 mmol l-1 after 24 h. Extracellular pH was compensated to only about 30% of the shift expected at constant bicarbonate level and, according to the steady reduction of pH, non-bicarbonate buffering of CO2 also contributed significantly to the elevation of bicarbonate. This relatively poor pH compensation (compared with fishes) could not be improved either by direct administration of bicarbonate into the bloodstream or by increased environmental ion concentrations. It is concluded that the availability of bicarbonate is not a limiting factor for pH compensation during hypercapnia, and that the inability of Bufo to accumulate bicarbonate to concentrations sufficient for better hypercapnia compensation is based on a constitutional 'bicarbonate threshold' of the resorbing and retaining structures for acid-base-relevant ions.
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PMID:Acid-base regulation and blood gases in the anuran amphibian, Bufo marinus, during environmental hypercapnia. 312 28

To evaluate the possible effect of induced hypercapnia on anaerobic metabolic rate during anoxia, musk turtles (Sternotherus odoratus) were submerged in N2-equilibrated water at 10 degrees C for 3 days either with (anoxic hypercapnic) or without (anoxic normocapnic) elevated aquatic PCO2 (30-40 Torr). Control animals had access to air at 10 degrees C. Plasma [lactate] was significantly higher (P less than 0.01) in the normocapnic [59.4 +/- 7.4 (SD) mM; n = 22] than in the hypercapnic (47.4 +/- 8.5 mM; n = 19) anoxic turtles, although the hypercapnic turtles had lower blood pH (P less than 0.05). Plasma ion concentrations (Na, K, Cl, Ca, and Mg), however, were no different in the two groups, although all values other than Na were different from control. In some of the animals, [lactate] and [glycogen] (per g wet wt) of skeletal muscle, heart, and liver were measured in addition to blood acid-base values and lactate. Tissue lactates, although significantly elevated from control, and glycogens, although (with the exception of skeletal muscle) significantly reduced from control, were no different in the two anoxic groups. We suggest that these tissue data are more valid indicators of anaerobic metabolic rate than is plasma lactate and therefore conclude that induced hypercapnia does not significantly depress anaerobiosis in musk turtles at 10 degrees C.
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PMID:Effect of induced hypercapnia on anaerobic metabolic rate of anoxic musk turtles. 313 62

We measured ventilatory responses to progressive isocapnic hypoxia and to hyperoxic hypercapnia (CO2) using rebreathing techniques in 16 parents of infants with autopsy-confirmed sudden infant death syndrome (SIDS) and 18 control parents matched for age, sex, and body size. Response to ventilatory loading was assessed by repeating the CO2 test with an inspiratory flow-resistive load (16 cm H2O/L/sec). During loaded and unloaded CO2 tests, respiratory effort was also assessed by measuring the pressure generated in the first 0.1 second (P0.1) of the subsequent inspiratory effort after brief manual occlusion of the inspiratory line. Ventilatory responses of the parents of victims of SIDS to chemical and mechanical stimulation were not significantly different from those of control parents. Responses in both groups were similar to previously reported normal values. There was a linear increase in ventilation (VE) in response to hypercapnia and hypoxia and in P0.1 in response to hypercapnia. We found expected increases in P0.1/PCO2 and decreases in VE/PCO2 slopes during loaded breathing in all subjects, but no difference between groups. We conclude that parents of SIDS victims have normal ventilatory chemosensitivity and respiratory drive.
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PMID:Ventilatory chemosensitivity in parents of infants with sudden infant death syndrome. 313 76

The preceding report on the O2 uptake (MO2) of chicken embryos whose shell conductance (GO2) was altered from the beginning of incubation showed that the MO2 was decreased despite increased GO2 [Okuda, A. and H. Tazawa (1988) Respir. Physiol. 74: 187-198]. This was attributed to an excess water loss which reduced the growth of the embryos. The present study was designed to investigate the short-term effects of altered GO2, obviating the effect of excess water loss, on the MO2 and simultaneously on the hematological variables of embryos on days 16-17 and days 18-19 of incubation. The MO2 measured 5 h after increasing the GO2 was neither decreased nor increased significantly. The diffusing capacity of the chorio-allantoic membrane, which was estimated using the Bohr integration procedure, decreased as the GO2 was increased. When the GO2 was decreased, on the other hand, the decrease in MO2 was not so large as expected from the decrease in GO2, for both 16- and 18-day-old embryos. The effect of reduced GO2 on MO2 was more prominent in 18-day-old embryos than 16-day-old embryos. One-day-long hypoxia due to decreased GO2 induced erythropoiesis in 18-19-day embryos, but did not do so in 16-17-day embryos. The increase in hematocrit value of the latter group of embryos was attributed to an increase in cell volume due to concurrent hypercapnia.
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PMID:Short-term effects of altered shell conductance on oxygen uptake and hematological variables of late chicken embryos. 322 77

Sleep apnea syndrome (SAS) is a rare disorder which is being diagnosed more often with increasing knowledge among physicians and patients. SAS presents with daytime hypersomnolence, intellectual deterioration and personality changes, chiefly in obese men, and is caused by intermittent upper airway obstruction during sleep at the level of the mesopharynx. Consecutive repetitive apneas of more than 10 seconds' duration are immediately abolished by pneumatic splinting with continuous positive pressure of 5 to 15 cm H2O with a nasal mask (nCPAP). A case report on a 31-year-old man with obesity and hypercapnia demonstrates that, although nCPAP by itself does not lead to weight reduction, it is more acceptable than surgical therapy (tracheostomy or uvulopalatopharyngoplasty).
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PMID:[Continuous nasal positive pressure respiration (nCPAP) as a therapeutic possibility in the sleep apnea syndrome]. 327 74

We report on the effect of the excised and grafted chest and abdominal burn on lung function. Six consecutive patients with 3 degree burns to the entire chest and abdomen (72 +/- 10% total body surface area 3 degree burns) were studied. A severe restrictive lung dysfunction due to the noncompliant nature of the excised and grafted chest and abdominal wound was identified; this was most evident when inspiratory pressure (IP) was even modestly impaired with general anesthetics. Measured vital capacity (VC) was 12 to 14 ml/kg at 6 to 8 wk postburn, in the absence of any significant parenchymal injury. The measured VC was identical to the tidal volume (VT) used during the extended period of mechanical ventilatory support. Dynamic compliance (or characteristic) (Cdyn) decreased dramatically from 35 +/- 8 to 15 +/- 9 ml/cm H2O when the positive pressure VT was increased by as little as 100 ml above prior VT settings, indicating the noncompliant nature of the combined chest and abdominal excised and grafted burn. Major cardiopulmonary complications developed in the first two patients after onset of the restrictive process when general anesthesia was used for grafting procedures (n = 8) and the limits of chest wall excursion were unrecognized. Patients received only continuous positive airway pressure preoperatively. A modest but significant decrease in IP from -45 +/- 8 to -33 +/- 5 cm H2O and 30% decrease in spontaneous VT were noted in the early postoperative period. These changes, however, resulted in a dramatic decrease in pulmonary function leading to hypercarbia, PCO2 greater than 50 torr.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Restrictive pulmonary dysfunction caused by the grafted chest and abdominal burn. 329 15

Persons with alveolar hypoventilation have abnormal daytime arterial blood gases and abnormal responses to hypercapnia and hypoxia in the absence of any identifiable lung or neuromuscular disease. The underlying defect in the control of breathing has not, however, been confirmed. We studied a 6-yr-old girl who was admitted in respiratory failure after a long history of disturbed breathing awake and asleep, which had been diagnosed as primary alveolar hypoventilation, (PaCO2 = 120). After several days of endotracheal intubation and assisted ventilation, her condition improved and she was extubated. At this time her ventilatory response to hypoxia was absent (VE/SaO2:0.1 l/min/% at a CO2 of 45) and there was a right-shifted response to hypercapnia (VE/PaCO2:2.6 l/min/mmHg). As obstructive sleep apnea was suspected, nocturnal nasal continuous positive airway pressure (CPAP) was tried; however, it was not effective in maintaining arterial oxyhemoglobin saturation. Definite central apneas were observed during sleep both with and without nasal CPAP, and there was an absence of snoring. Her condition deteriorated, and there was a progressive increase in her awake arterial CO2 levels for a period of 4 wk. The IPPV with 5 cm H2O of PEEP was administered through a nose mask during sleep and this maintained both oxygen saturation and transcutaneous CO2 levels within the normal range. After 10 days of nocturnal assisted ventilation, the hypercapnic response returned to the normal position (VE/CO2:2.1 l/min/mmHg).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Treatment of alveolar hypoventilation in a six-year-old girl with intermittent positive pressure ventilation through a nose mask. 330 Apr 41

To evaluate the role of the cerebral cortex in the response to externally added inspiratory flow-resistive load, we studied 7 patients manifesting clinical presenile dementia of the Alzheimer's type. All subjects exhibited diffuse cerebral cortical atrophy on computerized tomography of the brain. The mean age of the group was 45.6 yr. The rebreathing technique was used to assess minute ventilation (VE) and occlusion pressure (P100) responses to progressive hypercapnia. Rebreathing runs were performed before and during the addition of an inspiratory flow-resistive load of 18 cm H2O.L-1.s. The respiratory control data of these patients were compared with data obtained by similar techniques in a matched normal volunteer control group. In the patient group, with the addition of load, the VE/PCO2 response slope decreased (p less than 0.005), whereas the P100/PCO2 response slope did not significantly change. In the control group, P100/PCO2 response slope increased with load to maintain ventilation. These results suggest that in presenile dementia, during added inspiratory load, the drop in VE is associated with an inadequate increase in respiratory neuromuscular output. This lack of load compensation in patients with presenile dementia suggests a role for the cerebral cortex in the response to externally added load.
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PMID:Respiratory control in presenile dementia. 333 57


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